The UC College of Medicine is continuing its upward path in cutting-edge research to enhance discovery sciences and facilitate translation of these discoveries to improve health and clinical care while recruiting new faculty. The new undergraduate program fosters scientific curiosity and investigation for our students. We are creating an environment of advanced clinical care that surpasses any in the region.

The Center for Integrative Health and Wellness promotes the value of treating the whole person and works to provide evidence-based wellness initiatives across the Academic Health Center and into the community through education, research and clinical care.

The College of Medicine has identified four institutes in which we have outstanding quality, a track record of success, opportunities for funding and ability to advance translational research and deliver high-quality personalized care.

The University of Cincinnati College of Medicine is known for its strong educational programs. From medical degrees to summer research programs, the College of Medicine offers some of the most innovative and captivating science and research opportunities in the nation.

Public Relations and Communications

Latest News

UC Researchers Illustrate How Muscle Growth Inhibitor Is Activated

Published: 1/18/2018

CINCINNATI—Researchers at the University of Cincinnati
(UC) College of Medicine are part of an international team that has
identified how the inactive or latent form of GDF8, a signaling
protein also known as myostatin and responsible for limiting
muscle, is activated.

That knowledge could someday help in finding a better
treatment to improve muscle function in diseases such as muscular
dystrophy, amyotrophic lateral sclerosis (ALS) or Lou
Gehrig’s disease, and cancer cachexia, a muscle wasting
condition, says Tom Thompson, PhD, professor in the UC Department
of Molecular Genetics, Biochemistry and Microbiology. Muscular
Dystrophy is a hereditary condition marked by weakness and
progressive wasting of the muscles, while ALS impacts nerve
cells that control voluntary muscle movement.

The research team’s findings are detailed in a
peer-reviewed article in the scholarly journal for the Proceedings
of the National Academy of Sciences (PNAS). Thompson is the
corresponding author for the journal article, "
Molecular
Characterization of Latent GDF8 Reveals Mechanisms of
Activation,” and its first author, Ryan Walker, is a
postdoctoral fellow at Harvard University and a former UC doctoral
student who worked in Thompson’s laboratory. Also from UC
participating in the study are Jason McCoy, a doctoral student, and
Magdalena Czepnik, a research assistant.

"All animals have the protein molecule myostatin which limits
the size of our muscle,” explains Thompson. "Myostatin is
being targeted therapeutically to boost muscle production in
patients with muscle disorders.”

"Myostatin is one member in this very large family of
molecules that includes 33 ligands. They play very important roles
in many aspects of the human body and often are wrongly regulated
in many human diseases such as cancer. Some are used to develop
bone while others play large roles during in human
reproduction."

During synthesis, GDF8 or myostatin, is made as a precursor
which remains in a dormant state with half of the molecule holding
the section of GDF8 responsible for signaling inactive, says
Thompson. Activation involves slicing a section of the molecule
responsible for dormancy, thus allowing signaling to occur in
myostatin and inhibition of muscle growth. Researchers were able to
demonstrate that myostatin could be turned on with minor changes to
the molecule’s dormant mechanism.

"As researchers, our goal is to understand the details of how
these molecules are locked,” says Thompson, adding that they
will be using animal models to conduct this research. "By tweaking
the dormant state of the molecule, we can get myostatin to signal
without the need for cutting, basically picking the lock without a
key. Our study illustrates what parts of the dormant state are
important for holding GDF8 inactive and can be helpful in
understanding the mechanism for GDF8 signaling.”

Researchers from Monash University in Australia participating
in study include Adam Hagg, Paul Gregorevic, PhD, Craig Harrison,
PhD, and Kelly Walton, PhD. Richard Lee, MD, and Melanie Mills,
both of Harvard University, are participants in the study. Marko
Hyvönen, PhD, and Thomas Cotton, a doctoral student, both from the
University of Cambridge are part of the study.

Funding for this research came from the Muscular Dystrophy
Association, the National Institutes of Health, the American Heart
Association, the University of Cincinnati, and Australia’s
National Health and Medical Research Council.

Thompson is a consultant for Acceleron Pharma.

UC and Monash University have filed for intellectual property
for GDF8 and GDF11 listing Thompson, Walker and Harrison as
inventors. Harvard University and Brigham and Women’s
Hospital have filed for intellectual property on GDF11 listing Lee
as an inventor.